Jan H. Veldink

Aug 29, 2024 | nature.com | Oliver Harschnitz |Rianne de Jongh |Onur Basak |Kevin Talbot |Jan H. Veldink |Domino K. Schlegel | +1 more

AbstractIntermediate-length repeat expansions in ATAXIN-2 (ATXN2) are the strongest genetic risk factor for amyotrophic lateral sclerosis (ALS). At the molecular level, ATXN2 intermediate expansions enhance TDP-43 toxicity and pathology. However, whether this triggers ALS pathogenesis at the cellular and functional level remains unknown. Here, we combine patient-derived and mouse models to dissect the effects of ATXN2 intermediate expansions in an ALS background.

Jul 2, 2024 | nature.com | Alfredo Iacoangeli |Simon D. Topp |Puja R Mehta |Naomi Limbachiya |Kelly Williams |Wade K. Self | +15 more

Correction to: Nature Communications https://doi.org/10.1038/s41467-022-34620-y, published online 12 November 2022The original version of this Article contained an error in Figure 4. Under the heading ‘Disease duration (months)’, all disease durations were reported as ‘disease duration’ rather than reporting the numerical value. The correct version now reports the disease duration in months instead of the original, incorrect ‘disease duration’.